Compared with primary angle-closure glaucoma (PACG) patients without zonular laxity and the control group, there are differentially expressed molecules in PACG patients with zonular laxity, and a potential mechanistic network can be constructed therefrom.

This study investigates the pathogenesis of PACG by conducting multi-omics analyses of aqueous humor, blood and anterior lens capsule samples from PACG patients with and without concomitant zonular abnormalities, aiming to elucidate the etiology of zonular abnormalities and uncover novel mechanisms underlying their involvement in the pathogenesis of glaucoma.

Inclusion Criteria:

• Clinically diagnosed with primary angle-closure glaucoma (PACG)
• Aged ≥ 50 years, no gender restriction
• Case Group A: Undergoing glaucoma surgery with intraoperatively confirmed significant zonular laxity
• Case Group B: Undergoing glaucoma surgery with intraoperatively confirmed normal zonular morphology
• Control group: age- and sex-matched with case groups; clinically diagnosed with age-related cataract; normal anterior chamber depth and angle; no history or signs of glaucoma; undergoing cataract surgery

Exclusion Criteria:

• Secondary glaucoma
• History of previous intraocular surgery
• Systemic diseases that can cause abnormal ocular zonules
• Other severe ocular diseases
• Long-term use of medications affecting connective tissue metabolism

PACG patients with or without zonular laxity, as well as age-related cataract patients without a history or signs of glaucoma who served as the control group.